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Biomedical subjects

S Javaheri

Publications and source records attributed to S Javaheri.

At least 37 records · Page 2Linked to original sources
PubMed1993

Bumetanide decreases canine cerebrospinal fluid production. In vivo evidence for NaCl cotransport in the central nervous system.

Na/K/2Cl cotransport carrier plays an important role in fluid absorption and secretion in many epithelial tissues. The role of the carrier, however, in mammalian choroidal cerebrospinal fluid (CSF) production has been controversial. We used ventriculo-cisternal perfusion (VCP) labeled with blue dextran with or without bumetanide and measured choroidal CSF production in anesthetized, and paralyzed, mechanically ventilated dogs. During 3 h of VCP, mean intracerebroventricular and arterial pressures, PaCO2, pH, [HCO3-], and serum osmolality remained normal in both groups (n = 9 in each group). Beginning 90 min after the start of VCP, choroidal CSF production was measured every 15 min. In group I (control group), values for CSF production (means +/- SD) were 49 +/- 20, 49 +/- 21, 51 +/- 21, 51 +/- 23, 48 +/- 20, 56 +/- 24, and 48 +/- 20 microliters/min, at 90, 105, 120, 135, 150, 165, and 180 min, respectively. These values did not differ significantly from each other. In group II (bumetanide group), after baseline control CSF production had been determined at 90 and 105 min, bumetanide (10(-4) mol/liter) was added to VCP. Mean values for CSF production were 54 +/- 15 and 52 +/- 17 microliters/min before, and 39 +/- 25, 34 +/- 19, 28 +/- 10, 30 +/- 17, and 30 +/- 18 microliters/min after addition of bumetanide at 90, 105, 120, 135, 150, 165, and 180 min, respectively. Comparing the two groups, baseline values for CSF production measured at 90 and 105 min did not differ significantly. After addition of bumetanide (group II), however, decrements in CSF production varied from 30 +/- 27% at 120 min to 47 +/- 14% at 150 min, which were significantly different from changes in group I. The results of this study indicate that NaCl cotransport carrier is involved in secretion of CSF in dogs, and inhibition of the transporter results in approximately 50% reduction in CSF production.

Animals↗
PubMed1992

Lung function, breathing pattern, and gas exchange in interstitial lung disease.

BACKGROUND: The aim of this study was to determine the relation between the severity of abnormalities in ventilatory function tests and tidal breathing pattern and gas exchange indices in interstitial lung disease. METHODS: Pulmonary function, ventilation, carbon dioxide production, oxygen consumption, arterial blood gas tensions, and pH were measured during resting steady state conditions in 60 patients with proved interstitial lung disease. Patients were categorised by forced vital capacity (FVC) (percentage of predicted values) as having a mild, moderate, or severe restrictive defect with means (SD) of 71% (4%), 57% (4%), and 41% (7%) of predicted values, respectively. RESULTS: FVC varied from 29% to 79% of predicted values and from 0.99 l to 4.32 l. The two measurements of FVC correlated strongly with most static lung volumes and with transfer factor for carbon monoxide. Mean respiratory rates (per minute) and tidal volumes (ml) were 17 (4) and 484 (131), 20 (4) and 460 (139), and 23 (5) and 377 (109) in mild, moderate, and severe restrictive defects, respectively. FVC correlated negatively with respiratory rate and positively with tidal volume. Arterial carbon dioxide tension ranged from 30 to 49 mm Hg; only two patients were hypercapnic. Mean arterial oxygen tensions were not significantly different among the three groups, and there were no significant correlations between forced expiratory volume in one second or FVC and arterial carbon dioxide tension or carbon dioxide production. CONCLUSION: Low values of FVC were associated with increased respiratory rate and decreased tidal volume; this pattern of breathing mimics external elastic loading, suggesting that mechanoreceptors may contribute to the rapid and shallow pattern of breathing in interstitial lung disease. Hypercapnia seems to be rare in interstitial lung disease even when functional impairment is severe and tidal volume is small. The increased respiratory rate is important in maintaining adequate ventilation. In the face of a severe restrictive defect carbon dioxide production did not increase, which also contributed to the maintenance of eucapnia.

Carbon Dioxide↗
PubMed1992

Lack of effect of external warming on sleep architecture in sleep apnea/hypopnea syndrome.

Sleep apnea/hypopnea syndrome (SAHS) is characterized by nocturnal apneas (A) and/or hypopneas (H) occurring in various sleep stages. However, these disordered breathing events (DBE) occur rarely in slow-wave sleep (SWS) and are most severe in rapid eye movement (REM) sleep when severe hypoxemia results. Several studies have shown that a rise in body temperature by external warming, induced according to a specific protocol, affects normal human sleep architecture by diminishing the time spent in REM and increasing the time spent in SWS. The purpose of this study was to determine if external warming is as effective in sleep apneic patients in decreasing REM and increasing SWS, hoping that DBE and hypoxemia may diminish. Seven newly diagnosed patients were studied two more nights, on one of which (selected randomly) the sleep study was preceded by sitting in a warm bathtub with temperature of 41 degrees C for 1/2 h, 2 1/2 h before the start of sleep study. The mean maximum rise in oral temperature with warm bath was 2.0 +/- 0.4 degrees C. Total bed time (min) and sleep efficiency, REM, and SWS (%) were, respectively, 320 +/- 17 (SD), 81 +/- 8, 19 +/- 7, and 1.2 +/- 1.1 for the control (C) and 339 +/- 33, 79 +/- 11, 19 +/- 5, and 2.4 +/- 1.6 for the bath (B) night. In both C and B, the lowest O2 saturation (%) occurred in REM sleep and was 78 +/- 7 and 77 +/- 9, respectively. Comparing respective paired values between C and B, no significance was found.(ABSTRACT TRUNCATED AT 250 WORDS)

Baths↗
PubMed1992

Familial respiratory chemosensitivity does not predict hypercapnia of patients with sleep apnea-hypopnea syndrome.

The mechanisms of hypercapnia observed in some patients with sleep apnea-hypopnea syndrome (SAHS) are not known. In chronic obstructive lung disease (COLD), hypercapnic and hypoxic ventilatory responses (HCVR/HVR) are decreased in normal family members of hypercapnic patients compared with those of non-hypercapnic patients. This suggests a familial (presumably genetic) diminished chemosensitivity predisposing to hypercapnia. In this study we investigated the possibility of a similar mechanism in SAHS. Based on PaCO2, 29 patients with polysomnographic evidence of SAHS were divided into those with chronic hypercapnia (PaCO2 greater than or equal to 45 mm Hg, n = 13) and those with normocapnia (PaCO2 less than 45 mm Hg, n = 16). We studied healthy adult (greater than or equal to 17 yr) immediate family members of these patients. Family members were required to have normal spirometry and be on no medications. In Group I, there were 32 family members of hypercapnic patients and in Group II, 26 family members of normocapnic patients. In Group I, the mean (+/- SD) of age (yr) was 36 +/- 12, weight (kg) 82 +/- 22, FEV1 (L) 3.1 +/- 0.8, VCO2 (ml/min) 228 +/- 63, slope (L/min) of HCVR 2.0 +/- 0.8, and slope (L/min/1% saturation) of HVR -1.20 +/- 0.82. Respective values in Group II were 34 +/- 14, 83 +/- 16, 3.2 +/- 0.8, 233 +/- 63, 2.0 +/- 1.0, and -1.34 +/- 1.20. There were no statistically significant differences in measured variables between the two groups. Furthermore, there were no significant correlations between PaCO2 of patients and slopes of HCVR or HVR of their family members.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Role of NaCl cotransport in cerebrospinal fluid production: effects of loop diuretics.

Cerebrospinal fluid (CSF) is secreted primarily by the choroid plexus (CP) located in the cerebral ventricles. Although much is known about ionic composition of cisternal CSF, the mechanisms involved in secretion of CSF in mammals are still not understood. The main aim of this report is to critically review the role of NaCl cotransport carrier in CSF production. On the basis of the studies in the literature, a model for CSF production by the CP is proposed. In this model, CP cells are assumed to be equipped with an NaCl cotransport carrier located on the basolateral (blood-facing) membrane. Because Na+ and Cl- are the two principal ions in CSF, their continued secretions into cerebral ventricles by CP cells require an adequate intracellular supply, which may be guaranteed by the NaCl cotransport carrier. Although this appears to be a reasonable assumption, making the processes involved in CSF production similar to those of other secretory epithelial cells, the presence of such a carrier in mammalian CP remains controversial. The reasons for this controversy are critically reviewed, and some suggestions for further studies are made.

Animals↗
PubMed1990

Bumetanide and cerebrospinal fluid acid-base variables during acute CO2 elevation.

The purpose of this study was to investigate the effects of bumetanide, an inhibitor of NaCl cotransport on cisternal cerebral spinal fluid (CSF) acid-base balance during acute respiratory acidosis (ARA). We measured blood and CSF acid-base variables in two groups (N = 7 in each) of anesthetized paralyzed and mechanically ventilated dogs with bilateral ligation of renal pedicles (to eliminate saluresis). After baseline samples were obtained (-1 h) bumetanide (0.5 mg/kg) was administered intravenously within 15 min (group 2); group 1 received equal volume of diluted saline. ARA was induced 1 h later (0 h) and was maintained for 5 h. In both groups PaCO2 was maintained between 55 to 60 mm Hg. Mean cisternal CSF PCO2 was 42.8 +/- 2.6, and 43.8 +/- 2.5 mm Hg, respectively in group 1 and group 2 and rose approximately 20 mm Hg during ARA. In group 1, CSF [HCO3-] was 22.0 +/- 1.0, 24.8 +/- 0.6, and 25.4 +/- 1.6 mEq/L, respectively at 0, 2 1/2, and 5 h; respective values for group 2 were 22.9 +/- 1.5, 24.7 +/- 1.4, and 26.1 +/- 1.3 mEq/L. Comparing the two groups, respective values were not significantly different from each other. Similarly, between the two groups changes in CSF [Na(+)-Cl-] during ARA were not significantly different from each other. Based on our results we conclude that at the dose used in the present study bumetanide does not change ionic composition and acid-base balance of cisternal CSF when compared to controls. Because changes in CSF [Na(+)-Cl-] during ARA were similar in both groups, any inhibition of Cl- influx into CSF by bumetanide should have been proportional to that of Na+.

Acid-Base Equilibrium↗
PubMed1990

Effects of domperidone and medroxyprogesterone acetate on ventilation in man.

If endogenous dopamine acts as an inhibitory neurotransmitter in the carotid bodies in man, domperidone (DP), a selective dopamine D-2 receptor antagonist should stimulate carotid bodies and augment ventilation. Furthermore, the combination of a central ventilatory stimulant, medroxyprogesterone acetate (MPA), with a peripheral ventilatory stimulant, DP, may produce an additive/synergistic ventilatory effect. We conducted a double-blind, placebo-controlled (P), cross-over trial comparing MPA 20 mg three times daily (TID) and DP (20 mg TID) alone and together in 8 healthy male human subjects. Drug effects were measured after 7 days, and a two-week drug washout period was allowed. MPA significantly increased alveolar ventilation (VA), and slopes of hypercapnic and hypoxic ventilatory responses. Domperidone alone significantly increased the slope of the hypoxic response; however, VA and PaCO2 did not change significantly. The combination of MPA and DP resulted in ventilatory changes similar to MPA alone. We conclude that in man endogenous dopamine acts as a modulator of chemoreception during hypoxemia, but plays no major role tonically in control of ventilation during normoxemia and normocapnia. Lack of additive effect with combined DP and MPA suggests that these drugs may share the same final common pathway in the process of chemoreception.

Adult↗
PubMed1990

Lung function, hypoxic and hypercapnic ventilatory responses, and respiratory muscle strength in normal subjects taking oral theophylline.

Methylxanthines are known to be respiratory stimulants and are thought by some to augment hypercapnic and hypoxic ventilatory drive and improve respiratory muscle strength. Hypoxic and hypercapnic ventilatory responses were measured in 10 normal subjects before, during, and after administration of theophylline for three and a half days. Pulmonary function, carbon dioxide production, and mouth pressures during maximal static inspiratory and expiratory efforts were also measured. The mean (SD) serum theophylline concentration was 13.8 (3.2) mg/l. Lung volumes and flow rates did not change significantly with theophylline. The mean (SD) values for maximum static inspiratory pressure were 152 (27), 161 (25), and 160 (24) cm H2O, respectively before, during, and after theophylline. Neither these values nor peak expiratory pressure measurements were significantly changed. The slopes of the hypercapnic ventilatory responses were 2.9 (0.9), 3.3 (1.2), and 3.3 (1.4) l/min/mm Hg carbon dioxide tension (PCO2) respectively before, during, and after theophylline administration. The respective values for the slopes of the hypoxic response were -1.4 (0.9), -1.3 (0.8), and -1.1 (0.9) l/min/1% oxyhaemoglobin saturation. None of these values changed significantly with theophylline. Theophylline, however, increased carbon dioxide production (200 to 236 ml/min) and alveolar ventilation (4.7 to 5.7 l/min) significantly, with a concomitant fall of end tidal PCO2 (35.5 to 32.9 mm Hg). It is concluded that in man oral theophylline at therapeutic blood concentrations increases carbon dioxide production and ventilation without changing pulmonary function, respiratory muscle strength, or the hypoxic or hypercapnic ventilatory response significantly.

Adult↗
PubMed1990

Cheyne-Stokes respiration presenting as sleep apnea syndrome. Clinical and polysomnographic features.

This study reports polysomnographic features of five patients with Cheyne-Stokes respiration (CSR). They were referred for evaluation of presumptive sleep apnea syndrome on the basis of history and physical examination, but were found to have predominantly CSR on all-night sleep study. On the initial polysomnographic study, CSR comprised 47 to 86% of all disordered-breathing events. Cheyne-Stokes respiration resulted in considerable oxyhemoglobin desaturation (mean baseline saturation was 95 +/- 4 +/- SD, and lowest saturation was 76 +/- 8). More than one-half of all CSR events resulted in awakenings or arousals. Evidence of upper airway obstruction was noted in the majority of CSR events in three of five patients. Four patients were treated with theophylline; one who refused drug therapy was treated with nasal continuous positive airway pressure (CPAP). Comparison of sleep studies before and after therapy showed a significant decrease in the CSR index (29 +/- 11 versus 2 +/- 2) and in the maximal oxyhemoglobin desaturation associated with CSR (13 +/- 5 versus 3 +/- 2), and an improvement in lowest O2 saturation associated with CSR (76 +/- 8 versus 91 +/- 4). Total disruptions in sleep architecture per hour of sleep improved significantly with therapy (46 +/- 21 versus 20 +/- 8). We conclude that the clinical presentation of CSR can be indistinguishable from that of the "traditional" sleep apnea hypopnea syndrome and can result in major oxyhemoglobin desaturation and sleep fragmentation. Theophylline results in considerable improvement in the disordered breathing of CSR during sleep.

Cheyne-Stokes Respiration↗
PubMed1989

Increase in ventilation caused by aminophylline in the absence of changes in ventral medullary extracellular fluid pH and carbon dioxide tension.

A study was designed to investigate the possibility that changes in ventral medullary extracellular fluid carbon dioxide tension (PCO2) and hydrogen ion (H+) concentration mediate the ventilatory stimulation induced by systemic administration of aminophylline. Six cats with peripheral chemodenervation (bilateral carotid sinus nerve and vagal neurotomy) were studied while anaesthetised with chloralose urethane and breathing spontaneously at a regulated, constant, and somewhat raised end tidal PCO2. Variables were measured during steady state normoxaemia and 10 and 30 minutes after administration of 17 mg/kg aminophylline (mean (SD) blood concentration of theophylline 14.2 (1.5) mg/l). Aminophylline resulted in a significant and considerable increase in minute ventilation to 155% and 167% above baseline at 10 and 30 minutes. Mean (SD) values for arterial PCO2 were 5.6 (0.6), 5.6 (0.6), and 5.4 (0.6) kPa at 0, 10, and 30 minutes. Values for the ventral medullary extracellular fluid PCO2 were 7.6 (1.1), 7.5 (1.0), and 7.4 (1.0) kPa and for H+ concentration 62.7 (9.3), 62.6 (9.3), and 63.5 (8.0) nmol/l at 0, 10, and 30 minutes. After aminophylline infusion the PCO2 and H+ concentration of the extracellular fluid did not differ significantly from baseline values. It is concluded that in spontaneously breathing, peripherally chemodenervated cats the considerable increase in ventilation that follows an infusion of aminophylline is not mediated by change in the ventral medullary extracellular fluid PCO2 or hydrogen ion concentration.

Aminophylline↗
PubMed1989

Furosemide and cerebrospinal fluid ions during acute respiratory acidosis.

The purpose of this study was to investigate the effects of furosemide, an inhibitor of NaCl cotransport, on cisternal cerebrospinal fluid (CSF) acid-base balance during acute respiratory acidosis (ARA). We measured blood and CSF acid-base variables in two groups (n = 7 in each) of anesthetized, paralyzed, and mechanically ventilated dogs with bilateral ligation of renal pedicles (to eliminate saluresis). After base-line samples were obtained (-1 h), furosemide (50 mg/kg) was administered intravenously within 15 min (group II); group I received an equal volume of half-normal saline. ARA was induced 1 h later (0 h) and arterial CO2 tension was maintained between 55 and 60 Torr for 5 h. Mean cisternal CSF PCO2 was 42.8 +/- 2.6 and 39.5 +/- 1.7 Torr, respectively in groups I and II and rose approximately 20 Torr during ARA. In group I, CSF [HCO3-] was 22.0 +/- 1.0, 24.8 +/- 0.6, and 25.4 +/- 1.6 meq/l, respectively at 0, 2.5, and 5 h. Respective values for group II were 22.2 +/- 1.3, 24.3 +/- 1.8, and 24.6 +/- 1.0 meq/l. These values were not significantly different from each other. In each group, CSF [Na+-Cl-] increased significantly during ARA, but the changes were not significantly different when the two groups were compared. We conclude that furosemide at the dose used in the present study does not change ionic composition and acid-base balance of cisternal CSF compared with control. Because changes in CSF [Na+-Cl-] during ARA were similar in both groups, any inhibition of Cl- influx into CSF by furosemide should have been proportional to that of Na+.

Acid-Base Equilibrium↗
PubMed1988

Effects of aminophylline on hypoxemia-induced ventilatory depression in the cat.

We designed experiments to evaluate changes in ventral medullary (VM) extracellular fluid (ECF) PCO2 and pH during hypoxemia-induced ventilatory depression (VD). Our aim was to investigate effects of aminophylline on VD and VM ECF acid-base variables. We used aminophylline because it inhibits adenosine, which is released within the brain during hypoxemia and could mediate VD. Experiments were performed in seven cats with acute bilateral denervation of carotid sinus nerves and vagi. Cats were anesthetized with chloralose-urethan and breathed spontaneously at a regulated and elevated arterial PCO2 (PaCO2). Measurements were made during normoxemia, hypoxemia, and recovery before (phase I) and after (phase II) aminophylline. By use of strict criteria for definition of VD, during phase II two kinds of responses were observed. Aminophylline prevented VD in five cats. In these cats in phase I, with mean arterial PO2 (PaO2) = 105 and PaCO2 = 42.2 Torr, VM ECF PCO2, [H+], and [HCO3-] were 59.5 +/- 8.6 Torr (mean +/- SD), 60.2 +/- 9.4 neq/l, and 23.1 +/- 3.7 meq/l, respectively. When mean PaO2 dropped to 49 Torr, ventilation decreased 21%, with only small changes in VM ECF acid-base variables. Studies were repeated 30 min after aminophylline (17 mg/kg iv). In phase II, during normoxemia (PaO2 = 110 Torr) VM ECF Pco2, [H+], and [HCO3-] were 55.4 +/- 8.1 Torr, 62.0 +/- 8.0 neq/l and 20.7 +/- 2.5 meq/l, respectively. During hypoxemia (PaO2 = 48 +/- 4 Torr) mean ventilation, VM ECF PCO2, [H+], and [HCO3-] did not change significantly.(ABSTRACT TRUNCATED AT 250 WORDS)

Aminophylline↗
PubMed1988

Albuterol has no effect on diaphragmatic fatigue in humans.

Diaphragmatic fatigue may play an important role in precipitating acute respiratory failure. Pharmacologically, theophylline and beta-2 agonists have been used to improve diaphragmatic contractility. We designed experiments to study the effects of albuterol, a beta-2 agonist, on diaphragmatic fatigue in humans. In 5 normal subjects, fatigue was induced by breathing through an inspiratory resistance. Studies were done at 2 levels of diaphragmatic tension-time index (TTdi) of 0.25 and 0.30. At each TTdi, either placebo or albuterol (4 mg three times daily) was taken for 3 days. All subjects experienced side effects of sympathetic stimulation. Albuterol did not significantly increase the strength of the fresh diaphragm. With a TTdi of 0.25, values for mean endurance time were 649 +/- 250 (mean +/- SE) and 552 +/- 161 s, respectively, in placebo and albuterol runs. Respective values for TTdi of 0.30 were 109 +/- 14 and 143 +/- 27 s. During recovery, the mean values for the time needed for maximal transdiaphragmatic pressure (Pdimax) to reach 90% of the prefatigue Pdimax were 891 +/- 370 and 1043 +/- 394 s, respectively, for placebo and albuterol runs (TTdi = 0.25). Respective values for TTdi of 0.30 were 219 +/- 57 and 231 +/- 108 s. We conclude that, in humans, albuterol has no significant effect on the strength of the fresh or fatigued diaphragm, diaphragm endurance time, or the recovery of Pdimax from fatigue.

Adult↗
PubMed1987

Use of a modified Swan-Ganz pacing catheter for measuring Pdi and diaphragmatic EMG.

Measurements of pressures across the diaphragm (Pdi) and diaphragmatic electromyogram (EMG) have become an integral tool to study respiratory muscle fatigue. To measure Pdi and diaphragmatic EMG, three balloon catheter systems have to be swallowed; two of these measure esophageal and gastric pressures and the third one, usually a Swan-Ganz catheter records diaphragmatic EMG. In the present study we describe how a thermodilution Swan-Ganz pacing catheter can be very simply modified to measure both Pdi and diaphragm EMG. Because only one catheter has to be swallowed, subject's acceptability improves, particularly for repeated measurements in the same subject. We have used such a catheter system for more than 18 months to study respiratory muscle fatigue in man. The measurements of Pdi by the modified Swan-Ganz catheter compare well with those recorded simultaneously with conventional balloons, and in vitro frequency response measurements showed that amplitude responses differed by 2% at 2 1/2 Hz. Phase responses of the esophageal and gastric balloons were linear over the range of frequencies tested.

Catheterization↗
PubMed1987

Sodium salicylate has no effect on cerebrospinal fluid [H+] in dogs with normal acid-base balance.

The experiments described here were designed to investigate the possibility that central stimulation of respiration by salicylates may be due to changes in [H+] of cerebral fluids. Two groups (n = 6 in each) of anesthetized, paralyzed, and mechanically ventilated dogs were studied for 6 hr. Renal pedicles were ligated to maintain blood salicylate level constant. Group II received 150 mg/kg Na salicylate intravenously at 0 hr after samples had been obtained. Group I (control) received equal volume of half-normal saline. Mean plasma salicylate levels were 18.9, 18.4, and 19.6 mg % at 0.5, 3, and 6 hr after administration of Na salicylate. Respective cisternal cerebrospinal fluid (CSF) levels were 3.2, 4.8, and 5.9 mg %. Salicylate-induced hyperthermia was prevented by peritoneal cold dialysis, and a rise in PaCO2 was prevented by increasing ventilation. During the 6 hr of relatively normal systemic acid-base balance, cisternal CSF mean PCO2 values were 45.3, 43.6, and 49.3 mm Hg at 0, 3, and 6 hr in the control group; in group II, respective values were 46.9, 45.7, and 47.7 mm Hg. Cisternal CSF [H+] were 44.4, 45.2, and 50.5 nEq/L in group I at 0, 3, and 6 hr. Respective values in group II were 45.0, 47.5, and 50.6 nEq/L. These values were similar and statistically insignificant from those in group I. In both groups cisternal CSF [HCO3-] fell about 2 and CSF lactate concentration rose about 1 mEq/L at 6 hr.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗